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PubMed1981

Evidence for a folic acid binding protein in human cell membrane.

Cell membranes were prepared by sucrose discontinuous gradient from human liver and human peripheral leukocytes and erythrocytes and from circulating leukocytes from patients with chronic granulocytic leukemia (CGL) and acute myeloblastic leukemia (AML). The membrane preparations from liver and from leukemic leukocytes were shown to bind tritiated folic acid. The membranes from normal leukocytes and erythrocytes did not show this binding capacity. The membrane preparation from liver and CGL leukocytes showed two peaks of binding eluting with proteins from Sephadex G-200. However, protein extracts of these membrane preparations showed only a single peak for labelled folic acid, eluting near but just after albumin. The binding capacity of the membranes for folic acid was partially inhibited by reduced folate analogues. It is concluded that the liver plasma cell membrane and the membranes of myeloblasts in AML and circulating leukocytes in CGL contain a binding protein for folic acid which may be concerned in the transport of folates into these cells.

Animals↗
PubMed2003

Sex-related differences in procarbazine-induced cleft palate and microgenia and the anti-teratogenic effect of prenatal folic acid supplementation in rats.

Sex-related differences in the frequency of cleft palates and microgenia in rat fetuses prenatally treated with procarbazine (200 mg/kg on day 14 of gestation (GD14), group 1), and the anti-teratogenic effect of prenatal folic acid supplementation (4 mg/kg on GD14 through GD17, group 2) were studied in LEW.1A rats. In group 1, complete clefts were observed in 69% of the male and in 36% of the female fetuses while incomplete clefts (present only in the hard palate) were exhibited by 31% of the males and 43% of the females. Microgenia occurred in all males but only in 64% of the female fetuses. In group 2, the prenatal folic acid supplementation significantly reduced the occurrence frequency of complete clefts to 9% in males and to 0% in females. In contrast, incomplete clefts increased to 82% in males and 91% in females. Microgenias were reduced to 73% and 57% in male and female fetuses, respectively. Since incomplete clefts present in the hard palate are assumed to be residues of spontaneous intra-uterine repair processes of exogenously induced complete palatal clefts, we conclude that prenatal supplementation with folic acid at a dose of 4 mg/kg promotes the intra-uterine repair of cleft palates and offers a partial protection against procarbazine teratogenicity. Furthermore, it is deduced that gender-specific differences exist in the susceptibility to procarbazine and in the anti-teratogenic effect of folic acid on procarbazine-induced microgenia.

Animals↗
PubMed1978

Identification of methotrexate and folic acid analogs by mass spectrometry.

Methotrexate and folic acid analogs are polar molecules and attempts to obtain electron impact and chemical ionization mass spectra of these compounds by several laboratories have failed. We have found that methylation of this important class of compounds with diazomethane produces derivatives which are sufficiently volatile to allow their mass spectra to be recorded. The mass spectra of the methyl derivatives of five compounds, 4-amino-4-deoxy-N10-methylpteroylglutamic acid, 4-amimo-4-deoxypteroylglutamic acid, pteroylglutamic acid, 4-amino-4-deoxypteroic acid and N10-methylpteroylglutamic acid are presented, and the fragmentation pathways of these compounds discussed.

Folic Acid↗
PubMedDate not supplied

[Case report of a nutrition-induced anemia due to folic acid deficiency].

Because of anaemia and dystrophy a girl was admitted to hospital. By bone marrow aspiration the diagnosis of a megalocytic anaemia was established. The determination of folic acid revealed a severe folate deficiency caused by education problems with consecutive malnutrition. Under folic acid replacement therapy and intensive talks with the parents the girl recovered from her illness and after change of nutrition she developed well without any further folic acid replacement.

Anemia, Megaloblastic↗
PubMed2005

Reduction of the efficacy of antifolate antimalarial therapy by folic acid supplementation.

Malaria and anemia are common conditions in patients presenting to outpatient clinics in Kenya. Anemia is usually due to malaria infection with underlying micronutrient deficiency. Iron therapy has been shown to enhance recovery from anemia in children with malaria, without affecting malaria treatment. Iron and folic acid are often prescribed together for anemic individuals. Until recently in Kenya, the drug of first choice for non-severe malaria was sulfadoxine-pyrimethamine (SP), an antifolate antimalarial drug. In this study, 303 patients of all ages with anemia and uncomplicated Plasmodium falciparum malaria attending an outpatient clinic in an area of seasonal malaria were treated with SP and iron, and were randomized to receive folic acid. Parasite clearance rates were measured using a survival analysis plot for both parasitologic and clinical failure. There was a significant reduction in the efficacy of SP in patients taking standard therapeutic doses of folic acid using the survival curve for parasitologic failure (P < 0.0001), but no difference for clinical failure (P = 0.7008). Folic acid supplementation did not enhance recovery from anemia.

Anemia↗
PubMed1977

The bioavailability of folic acid added to wine.

Folate deficiency is a frequent cause of anemia in alcoholics, but little attention has been paid to its prevention. Folic acid was readily soluble in wines of high ethanol content at concentrations of 10 microgram/ml. Lactobacillus casei folate activity of folic acid added to wines was well maintained during a month's storage at room temperature and fell to 61% to 66% of original activity after 3 months. Pteroylglutamic acid, 10 microgram/ml, added to wines and given in doses of the beverages (4 ml/kg body weight that caused inebriation, was well absorbed by six normal human volunteers (mean maximal increment in serum folate concentration +/- SEM, 71 +/- 8 ng/ml) and by seven recently intoxicated chronic alcoholics (mean increment, 94 +/- 4 ng/ml). Folate deficiency in alcoholics could be prevented by the fortification of alcoholic beverages with the vitamin.

Adult↗
PubMed1975

[Frequent and rare forms of vitamin B 12 and folic acid deficiency anemias].

The common and rarer causes of vitamin B12 and folic acid deficiency are discussed with special reference to pathophysiological aspects and conditions in Switzerland. The overall incidence of Addisonian pernicious anemia was found to be 80 per 100,000 patients, whereas the incidence of other B12 deficiency states was 18 per 100,000 patients. Folic acid deficiency was found in 23 of 100,000 patients, though this figure appears to be an underestimate. Nutritional (latent) folate deficiency seems to be the most frequent vitamin deficiency in Switzerland.

Anemia, Pernicious↗
PubMed1996

Augmentation of the therapeutic activity of lometrexol -(6-R)5,10-dideazatetrahydrofolate- by oral folic acid.

Recent clinical trials with lometrexol [(6R)-5,10-dideazatetrahydrofolate] have revealed a level of toxicity in humans that was not predicted on the basis of previous in vivo preclinical studies. Because standard laboratory animal diets contain high levels of folic acid relative to human folate intake, the toxicity and therapeutic activity of lometrexol was studied in mice under conditions of restricted dietary folate intake. Remarkably, the lethality of this drug increased by three orders of magnitude in mildly folate-deficient mice, mimicking the unexpected toxicity seen in humans. Lometrexol had limited therapeutic activity in folate-deficient mice bearing the C3H mammary adenocarcinoma, compared with the substantial therapeutic index for treatment of this tumor in animals on standard diet. When folic acid was administered p.o. to mice that were mildly folate deficient, antitumor activity was again observed at nontoxic doses of lometrexol, and the range of lometrexol doses that allowed safe therapeutic use of this drug increased at higher dietary folate intake. At a fixed dose of lometrexol, the antitumor effects in animals were dependent on the level of dietary folate and went through a distinct optimum. Excessively high folate intake reversed the antitumor effects of lometrexol. Optimization of the folic acid content in the diet and of the lometrexol dosage are predicted to have substantial impact on the clinical activity of this class of drugs.

Adenocarcinoma↗
PubMed1983

Brain atrophy, peripheral neuropathy and folic acid deficiency.

A woman with peripheral neuropathy and cerebral atrophy, both secondary to a selective folic acid deficiency caused by severe gastrointestinal disturbances, was given folic acid replacement therapy, which improved her clinical, blood and neurophysiological status.

Atrophy↗
PubMed1978

Effects of biotin, folic acid, and pantothenic acid on the growth of Mycoplasma meleagridis, a turkey pathogen.

The biotin, folic acid, and pantothenic acid requirements of Mycoplasma meleagridis were determined in vitro by examining the growth and survival of the organism in the presence of varying concentrations of these factors. Growth and survival were also studied in the presence of aminopterin and methotrexate which prevent utilization of folic acid, and in the presence of avidin, a known biotin antagonist. Whereas pantothenate appeared to have no obvious effect on growth or survival, folate was marginally stimulatory at only the highest concentration tested. Aminopterin exerted a slight, but not significant, inhibitory effect at four of the five concentrations tested. In contrast, the inhibition seen with methotrexate increased, dependent on dose. Biotin exerted a pronounced stimulatory effect at the two highest concentrations tested. Avidin inhibited growth only at one of the concentrations tested; however, this concentration did not correspond to the greatest amount of avidin. The possible significance of the avidin-biotin relationship to the etiology of Turkey Syndrome 1965 is explored on the basis of these in vitro observations and previous in vivo findings.

Aminopterin↗
PubMedDate not supplied

Cytochemical demonstration of folic acid in normal and leukemic granulocytes.

By means of an original cytochemical method, folic acid was demonstrated "in situ" in peripheral white blood cells in acute and chronic granulocytic leukemia. In control blood smears folic acid-relevant granules were found predominantly in the nuclei of neutrophils and basophils. Eosinophils were found positive for folic acid reaction both in nuclei and cytoplasm. In leukemic undifferentiated cells, less marked in acute than in chronic granulocytic leukemia, the cytoplasms contained a great quantity of folate. Nuclei were fewer or nonreactive. Therefore the cytochemical localization may be related to the degree of the white cells differentiation.

Folic Acid↗
PubMed2005

Effect of folic acid supplementation on mood and serotonin response in healthy males.

Evidence suggests that low folate status may be detrimental to mood and associated with depleted cerebrospinal fluid levels of the neurotransmitter serotonin (5-hydroxytryptamine; 5-HT). A placebo-controlled trial was carried out to determine the effect of folic acid supplementation (100 microg for 6 weeks followed by 200 microg for a further 6 weeks) upon subjective mood (Positive and Negative Affect Schedule) and biochemical markers of mood (5-HT) in healthy males (n 23). Blood samples were obtained at baseline (week 0) and during the intervention at week 6 and week 12. Subjective mood assessments were obtained at week 0 and week 12. The results showed an increase in serum and erythrocyte folate concentrations (P=0.02 and P=0.003, respectively) and a corresponding decrease in plasma homocysteine (P=0.015) in response to the folic acid intervention. Neither subjective mood nor 5-HT levels, however, were significantly altered in response to the change in folate status. Folic acid given at physiological doses did not appear to improve the mood of healthy folate-replete individuals over a 12-week period. Further research is needed to address the effect of folic acid supplementation or of longer duration or increased dose, particularly in the face of sub-optimal folate status.

Adult↗
PubMed1977

[Study of folic acid blood levels during estro-progestagen treatments].

When the blood levels of folates were estimated in 100 women following treatment with oestro-progestagens the following facts emerged : 1) There is no significant difference between the folate levels found in women on oestro-progestagens compared with a control population of the same age. 2) We have not found any evidence of frank folic acid deficiency in women on oestro-progestagens, but there have been slight drops in the levels of folates in women who show other reasons for folic acid deficiency than taking oral contraceptives. These are : troubles in absorption, salmonella, an increase in the need for folic acid in pregnancy, and failure of transport. Furthermore the incidence of lower levels in the control population was exactly the same as in the experimental population.

Contraceptives, Oral↗
PubMedDate not supplied

Dietary nickel and folic acid interact to affect folate and methionine metabolism in the rat.

A previous experiment using rats indicated that dietary nickel (Ni), folic acid, and their interaction affected variables associated with one-carbon metabolism. That study used diets that produced only mild folate deficiency. Thus, an experiment was performed to determine the effect of a severe folate deficiency on nickel deprivation in rats. A 2 x 2 factorially arranged experiment used groups of six weanling Sprague-Dawley rats. Dietary variables were nickel, as NiCl2-6H2O, 0 or 1 microgram/g and folic acid, 0 or 4 mg/kg. All diets contained 10 g succinylsulfathiazole/kg to suppress microbial folate synthesis. The basal diet contained < 20 ng Ni/g. After 58 d, an interaction between nickel and folate affected the urinary excretion of formiminoglutamic acid (FIGLU) and the liver concentration of S-adenosylmethionine (SAM). Because of this, it is proposed that the physiological function of nickel is related to the common metabolism shared by SAM and FIGLU. Possibly the physiological function of nickel could be related to the tissue concentration of 5-methyltetrahydrofolate (MTHF) or tetrahydrofolate (THF).

Animals↗
PubMed1994

Rapid translocation of myosin II in vegetative Dictyostelium amoebae during chemotactic stimulation by folic acid.

Immunofluorescence studies showed that cytoskeletons that were composed of actin and myosin II rapidly reorganized in vegetative Dictyostelium cells upon chemotactic stimulation by folic acid. The amount of F-actin increased biphasically with peaks at 5-10 sec (first peak) and 25-45 sec (second peak) after the addition of folic acid. Filaments of myosin II became associated with cell membrane with increases in the meshwork of actin filaments on the cell membrane at the time of the second peak. The number of actin foci in the actin meshwork on the cell membrane decreased transiently at the time of the second peak. The number of filaments of myosin II on the cell membrane decreased and the number of actin foci recovered concomitantly towards the end of the second peak. This reorganization of cytoskeletons during the chemotactic stimulation was also observed after the application of the calcium ionophore A23187 or cGMP to cells. These observations suggest that increases in intracellular levels of both Ca2+ ions and cGMP may play a crucial role in the rapid translocation of myosin II during stimulation by folic acid.

Actins↗
PubMed2003

[Serum homocysteine, vitamin B12 and folic acid concentrations in patients with alcoholic liver cirrhosis].

The aim of the work was to establish serum homocysteine, vitamin B12 and folic acid concentrations in patients with alcoholic liver disease. Mentioned above vitamins are enzymatic cofactors for metabolic changes of homocysteine. It is a common fact that alcoholics often present with avitaminosis. Additionally, damaged liver worsens this pathology what can negatively influence metabolism of homocysteine. 40 patients--(mean age 52.7 years) and 40 healthy individuals (mean age 50.3 years) were examined. Hyperhomocysteinemia (concentration > 12 mmol//l) was stated in 50% of the patients and mean homocysteine concentration was statistically significantly higher if compared to the controls (13.29 +/- 8.16 vs 11.03 +/- 1.6 mmol/l p < 0.05). In the female patients homocysteine concentration was significantly higher than in the healthy controls (14.6 +/- 10.63 vs 10.73 +/- 1.37 mmol/l p < 0.001). A negative correlation between homocysteine concentration and folic acid concentration in the group of the patients with hyperthomocysteinemia was observed (r = -0.88, p < 0.001) and among all the patients (r = -0.312, n.s.). Vitamin B12 levels were significantly higher in the group of patients than in the controls (659.43 +/- 489.27 vs 384.44 +/- 145.93 p < 0.001) what is consistent with the data from the literature. A positive correlation between mean homocysteine concentration, age and platelet count of the examined patients was stated (r = 0.350, p < 0.05, r = 0.508, p < 0.001). On the basis of the obtained results one can conclude that hyperthomocysteinemia is often established in alcoholic liver disease. Partially, low folic acid concentration is responsible for this fact. In theoretical deliberation one should consider estimation of betaine metylotransferasis levels--the enzyme which is responsible for homocysteine metabolism in the liver.

Female↗